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Diagnosa Penyakit Ginjal Kronik Dan Indikasi TPG RRT

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Dr Rubin Surachno

 Kidney damage for >= 3months ,


as defined by structural / functional abnormalities of
kidney
with or without decreased GFR,
and manifest by either :
 Pathologic abnormalities
 Markers of kidney damage, including abnormalities in
composition of blood / urine or abnormalities on imaging
 GFR < 60 ml/min/1.73m2 for >=3 months,
with / without kidney damage
 Family history of heritable renal disease
 Diabetes
 Hypertension
 Auto-immune disease
 Old age
 Prior episode of ARF
 Current evidence of renal damage, even with normal or
increased GFR
Cause Clinical Presentation

Diabetic kidney History of diabetes, proteinuria and retinopathy


disease
Hypertension Elevated BP, normal UA, family history

Non diabetic Nephritic or nephrotic presentations


glomerular
disease
Cystic kidney Urinary symptoms, abnormal sediment, radiologic
disease findings
Tubulointerstitial UTI, reflux, chronic med use, drugs, imaging
disease abnormalities, urine concentrating defects
 Final Common Pathway is loss of nephron mass

Structural/
Diabetes
Loss of Functional Mediated by
Hypertension
Nephron Hypertrophy vasoactive
Chronic GN
Mass of remnant molecules,
Cystic Disease
nephrons cytokines and
Tubulointerstitial
disease growth factors,
renin angiotensin
axis
Sclerosis
of remnant
nephrons
 By Radiology – USG / CT / MRI etc…

 By Histology – Renal Biopsy


 Microalbuminuria

 Proteinuria

 Hematuria esp associated with proteinuria

 Casts ( with cellular elements )


Cockcroft-Gault formula
Ccr (ml/min) = (140-age) x weight *0.85 if female
72 x Scr

MDRD Study equation


GFR (ml/min/1.73 m2) = 186 x (Scr)-1.154 x (age)-.203 x
(0.742 if female) x (1.210 if African American)
STAGE DESCRIPTION GFR ( ml/min/1.73m2 )

1 Kidney damage with >=90


normal / increased GFR

2 Kidney damage with 60 – 89


mildly decreased GFR

3 Moderately decreased GFR 30 – 59

4 Severely decreased GFR 15 – 29

5 Kidney failure < 15 / dialysis


STAGE ACTION PLAN

1 DIAGNOSIS AND TREATMENT


SLOW PROGRESSION

2 ESTIMATE PROGRESSION

3 EVALUATE AND TREAT


COMPLICATIONS

4 PREPARE FOR RENAL


REPLACEMENT THERAPY

5 RENAL REPLACEMENT
 Stage 1 and 2
 Asymptomatic, hypertension
 Stage 3 and 4
 Anemia – loss of energy
 Decreasing appetite; poor nutrition
 Abnormalities in Calcium, Phosphorus metabolism
 Sodium, water, potassium and acid base abnormalities
 Stage 5
 All of the above – accentuated; eventually overt uremia
 Diagnosis

 Measures to slow progression

 Estimate Progression

 Evaluation and Treatment of Complications

 Preparation for Renal Replacement Therapy


 History

 Physical Examination
CLINICAL FACTORS SOCIODEMOGRAPHIC FACTORS
DIABETES MELLITUS OLDER AGE
HYPERTENSION EXPOSURE TO CERTAIN CHEMICALS
/ ENVIRONMENTAL CONDITIONS
AUTOIMMUNE DISEASES LOW INCOME / EDUCATION
SYSTEMIC INFECTIONS
URINARY TRACT INFECTIONS
URINARY STONES
LOWER URINARY TRACT
OBSTRUCTION
NEOPLASIA
FAMILY HISTORY OF CKD
RECOVERY FROM AKI
REDUCTION IN KIDNEY MASS
DRUGS
LOW BIRTH WEIGHT
Tests & Diagnostics Significance / Goal
Blood Pressure < 130 / 80 mm Hg ; Use ACEI /ARB
Serum Creatinine To estimate GFR;
Historical values assist in determining
acuity and progression of disease
Urinalysis with microscopy Presence of RBCs / RBC casts and or
Proteinuria – further work up
Serum Electrolytes ( Na+, K+ ) Useful as crude surrogate of renal disease
Help to guide antihypertensives
Help to identify patients in need of
medical nutrition education
Calcium, Phosphorus, PTH, ALP, Assists in treatment of metabolic bone
25-OH VITAMIN D disease
Complete Blood Count Evaluate for anemia
Peripheral Blood Smear
TSAT , S.Ferritin Useful in evaluation of iron stores
Tests & Diagnostics Significance / Goals
Renal Ultrasound with or without Arterial Characterize Kidney number and size
Doppler Echogenicity of kidneys
Rule out presence of obstruction
Rule out renovascular disease
Cholesterol panel Especially useful for patients with
nephrotic range proteinuria
Random urine protein Ratio approximate values obtained by
Random urine creatinine 24 hour collection
Hepatitis Serology Negative Hep B testing mandates
vaccination
Serum Protein Electrophoresis In adults with renal disease to rule out
Urine Protein Electrophoresis Myeloma
Antinuclear antibody Warranted for adults with proteinuria /
evidence for SLE
HIV Warranted in selected population
Renal Biopsy Indicated in pts with hematuria and /
proteinuria and lack of evidence of
systemic disease
 Protein Restriction

 Reducing Intraglomerular Hypertension

 Reducing Proteinuria

 Control of Blood Glucose

 Control of Blood Pressure


 Reduces symptoms associated with uremia
 Slows the rate of decline in renal function at earlier stages of
renal diseases

 K/DOQI clinical practice guidelines recommend


daily protein intake between 0.60 – 0.75 g / Kg per day
 50 % of protein intake should be of high biological value

 As patient approaches CKD Stage V,


spontaneous protein intake decreases & patient enter a state of
Protein – Energy Malnutrition . Recommended protein intake is
0.9 g / Kg per day
 Increased intraglomerular filtration pressure & glomerular
hypertrophy - a response to loss of nephron number

 It promotes ongoing decline of kidney function even if the inciting


process has been treated.

 ACEI & ARBs

 Inhibit angiotensin induced vasoconstriction of efferent arteriole

 Reduces intraglomerular filtration pressure and proteinuria


 If monotherapy is not effective , combined therapy with
both ACEI & ARB can be tried

 2nd line drugs : Calcium Channel Blockers


Diltiazem , Verapamil

 Especially - Diabetic Nephropathy & Glomerular diseases


 Leading cause of Chronic Kidney Disease

 Control of Blood Glucose : excellent glycemic control


reduces the risk of kidney disease & its progression in
both Type 1 & 2 Diabetes Mellitus
 Recommendations : FBS : 90 – 130 mg/dl
HbA1C < 7%

 Control of Blood Pressure & Proteinuria : ACEI & ARBs


 Hypertension : sodium and water retention
renin angiotensin system activation

 Control of BP : to slow progression of CKD


to prevent extrarenal complications
( cardiovascular disease / stroke )

 Goal : BP < 130 / 80 mm Hg


BP < 125 / 75 mm Hg ( DM / Proteinuria > 1g/day )
 Salt Restriction
 Diuretics
 Loop Diuretics : Furosemide 40 mg BD
Bumetanide 1mg BD
 Thiazides : less efficacious gfr < 30 – 40 ml/min
 Both ameliorate hyperkalemia seen with ACEI / ARB
 ACEI / ARB
 Check S.Creat & S.K+ within 1 -2 weeks
 Upto 30 % increase in creatinine is acceptable
 Beta blockers / CCB / Alpha blockers / Vasodilators
 Anemia

 Bone Disorders

 Dyslipidemia

 Cardiovascular disease
 Defined as Hemoglobin < 13.5 g/dl in males
< 12 g/dl in females

 Normocytic normochromic anemia –


as early as in Stage III CKD or
universally by Stage IV CKD
 Primary cause : insufficient production of Erythropoetin
 Additional factors : iron deficiency
folate / vit B12 deficiency
chronic inflammation
hyperparathyroidism / bm fibrosis
 Target Hb : 11 g/dl

 Target Iron status : TSAT : lower limit > = 20


S.Ferritin : ng/ml
lower limit : 200 – HD CKD
100 – Non HD CKD
> 500 not routinely recommended
 Check Hb monthly while on ESAs
 Iron studies monthly when started on ESA
 On stable ESA Therapy : Iron studies can be done 3 monthly
 Ferrous sulphate 325 mg bid – tid
 IV Iron Dextran
 IV Iron Sucrose
 IV Sodium Ferric Gluconate Complex
 Folic acid and Vitamin B 12 supplements
 Erythropoetin Stimulating Agents : Epoetin alfa
Epoetin beta
Darbepoetin alfa
 Epoetin alfa / beta : 50 -100 IU / Kg SC per week
 Darbepoetin alfa : 40 mcg SC every 2 weeks
 Osteitis Fibrosa Cystica  Secondary
Hyperparathyroidism
 Osteomalacia  Vitamin D deficiency
 Acidosis
 Adynamic bone disease  Aluminium accumulation
 Osteoporosis in elderly
 Mixed osteodystrophy  Osteopenia caused by
steroids
 Renal bone disease – significantly increase mortality in
CKD patients

 Hyperphosphatemia – one of the most important risk


factors associated with cardiovascular disease in CKD
patients
 K/DOQI recommends :
 CKD Stage III & IV : S.Phosphorus : 2.7 - 4.6 mg / dl
 CKD Stage V : S.Phosphorus : 3.5 - 5.5 mg / dl

CKD STAGE GFR RANGE INTACT PTH ( pg/ml )

3 30 – 59 35 – 70

4 15 – 29 70 – 110

5 < 15 / Dialysis 150 – 300


CKD STAGE GFR RANGE PTH LEVELS S.Calcium &
S.Phosphorus
3 30 -59 Every 12 months Every 12 months
4 15-29 Every 3 months Every 3 months
5 < 15 / dialysis Every 3 months Every month
 Reduce dietary phosphate intake
 Phosphate binders : calcium carbonate
calcium acetate
aluminium hydroxide
magnesium carbonate ( rarely used )
sevelamer hydrochloride
lanthanum carbonate
 The use of calcium salts is limited by development of
hypercalcemia
 Calcium acetate poses a less problem as less calcium is
absorbed
 Calcimimetics – Cinacalcit :

 Agent that increase calcium sensitivity of the calcium


sensing receptor expressed by parathyroid gland
 Down regulating the parathyroid hormone secretion
 Reduce hyperplasia of parathyroid gland

 Calcitriol 0.25 mcg OD

 Paricalcitol 1 mcg daily or 2mcg 3 times a week


 Vitamin D deficiency :
 < 5 ng/ml – Ergocalciferol 50000 IU orally weekly for
12 weeks and then monthly thereafter

 5 – 15 ng/ml – Ergocalciferol 50000 IU orally weekly for


4 weeks and then monthly thereafter

 16 – 30 ng/ml – Monthly Ergocalciferol

 Acidosis : K/DOQI – total Co2 >=22 mEq/L


Sodium bicarbonate 650 – 1300 mg bid – tid
 A major risk factor for cardiovascular morbidity &
mortality

 Prevalence of hyperlipidemia increases as renal functions


diminish

 All patients with CKD must be evaluated for


Dyslipidemia

 Fasting lipid profile – annually


 Stage V CKD patients with dyslipidemia should always be
evaluated for secondary causes :
 Nephrotic syndrome
 Hypothyroidism
 Diabetes mellitus
 Excessive alcohol consumption
 Liver disease
 Drugs : oral contraceptives , haart etc…

 Goal : LDL – Cholesterol < 100 mg / dl


 LDL : 100 – 129 mg/dl : Lifestyle changes
Not responded : Low dose statin

 LDL >= 130 mg/dl : Lifestyle changes + Statins

 TG >= 200 mg/dl : Lifestyle changes + Statins


 Leading cause of
morbidity and mortality in
patients with CKD at all
stages
 Ischemic CAD
 Hypertension and LVH
 Congestive heart failure
 Uremic pericarditis
 Control BP : ACEI / ARB

 Treat dyslipidemia : Lifestyle changes + Statins

 Good Glycemic control

 Treat anemia

 Correct hyperphosphatemia

 Treat hyperparathyroidism

 Correct hyperkalemia
 Hepatitis B vaccination : 3 doses (0,1,2 months )
higher dose ( 40 mcg / ml )

 Pneumococcal vaccination : single dose


one time revaccination 5 yrs
after initial vaccination

 Influenza vaccination : recommended annually for adults


> 50 yrs age
 Patients of CKD Stage IV approaching Stage V should be referred
for
 Vascular access if hemodialysis is preferred
 Peritoneal dialysis catheter placement if peritoneal dialysis is
preferred

 AVF is most preferred access for HD patients


 Ideally created 6 months prior to start of HD
 Non dominant upper extremity
 And that arm is to be preserved – no iv lines

 AVG : 3-6 weeks prior to start of HD


 PD Catheter : 2 weeks prior to start of HD
MEDICAMENTOSA
(PREVENTION OF PROGRESSION OF RENAL DISEASE)

-Protein restricting diet ( 0.6-0.8 gr/kgBB/day)


-Blood pressure control
-Managing Fluid and Electrolyte disorders
-Managing hyperphosphatemia, hyperkalemia, etc)
-Treating anemia
-Managing hyperlipidemia

RENAL REPLACEMENT THERAPY


In cases of GFR reduced to < 10 – 15 cc/min (= s creat 8-10 mg/dl
or 20 cc/min in DM ( s creat 6-8 mg/dl)
 GFR not below 15 ml/min.1.73m2 but in presence of
 Intractable volume overload
 Hyperkalemia
 Hyperphosphatemia
 Hypercalcemia / Hypocalcemia
 Metabolic acidosis
 Anemia
 Uremic encephalopathy
 Uremic pericarditis
 Severe hypertension , acute pulmonary edema
DIALYSIS TRANSPLANTATION

HEMODIALYSIS LIVING DONOR

HEMOFILTRATION

PERITONEAL CADAVERIC DONOR


PERITONEAL DIALYSIS a dialysis process using peritoneum membrane
as the semi-permeable membrane for difusion dan filtration

PERITONEAL DIALYSIS TECHNIC

1.Dialisate (1-2 Liter) enter the peritoneum


Dialisate cavity via Peritoneal Cathether
enter 2.Dialysate kept for some hours
to allow the difusion & filtration process
3.Ultrafiltrate exit the cavity
Ultrafiltrate 4.Change with new dialisate
exit 5.Recycling every 4 -8 hours

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